An experimental drug called Ocrelizumab has shown promise in a Phase 2 clinical trial involving 220 people with multiple sclerosis (MS), an often debilitating, chronic autoimmune disease that affects an increasing number of people in North America. It usually strikes young adults and is more common in women than in men. The study, carried out by researchers at the University of California, San Francisco (UCSF) Medical Center, and involving hospitals in the United States, Canada, and Europe, was published online on November 1, 2011 in the British medical journal Lancet. The study involved patients with relapsing-remitting MS, a form of the disease marked by the accumulation of lesions in the brain and spinal cord and periodic “attacks” of neurological impairment. The 220 patients were randomly enrolled into four groups – two that received injections of the monoclonal antibody Ocrelizumab at two different doses, one that received the standard multiple sclerosis drug interferon-beta, and one “control” group that was given a placebo. The doctors gauged the effectiveness of each treatment by performing monthly magnetic resonance imaging (MRI) brain scans of the patients and counting the number of visible marks that indicate inflamed lesions, a hallmark of the disease. They also compared the severity and frequency of neurological “attacks” that cause loss of vision, incoordination, weakness and numbness, among other symptoms. The results of this trial showed that patients who received the drug generally fared well and showed fewer signs of the disease than patients who receive a placebo or the standard interferon treatment. Overall, the trial found that Ocrelizumab led to a 89 percent reduction in the formation of brain lesions, and it also reduced the number of new MS attacks over 24 weeks.

After more than a century of study, mysteries still remain about the process of meiosis—a special type of cell division that helps ensure genetic diversity in sexually-reproducing organisms. Now, researchers at Stowers Institute for Medical Research, in Kansas City, Missouri, shed light on an early and critical step in meiosis. The research, published online on October 27, 2011 in Current Biology, clarifies the role of key chromosomal regions called centromeres in the formation of a structure known as the synaptonemal complex (SC). "Understanding this and other mechanisms involved in meiosis is important because of the crucial role meiosis plays in normal reproduction—and the dire consequences of meiosis gone awry," says Dr. R. Scott Hawley, who led the research at Stowers. "Failure of the meiotic division is probably the most common cause of spontaneous abortion and causes a number of birth defects such Down syndrome," Dr. Hawley says. Meiosis reduces the number of chromosomes carried by an individual's regular cells by half, allocating precisely one copy of each chromosome to each egg or sperm cell and thus ensuring that the proper number of chromosomes is passed from parent to offspring. And because chromosomes come in pairs—23 sets in humans—the chromosomes must be properly matched up before they can be divided up. "Chromosome 1 from your dad has to be paired with chromosome 1 from your mom, chromosome 2 from your dad with chromosome 2 from your mom, and so on," Dr. Hawley explains, "and that's a real trick. There's no room for error; the first step of pairing is the most critical part of the meiotic process. You get that part wrong, and everything else is going to fail." The task is something like trying to find your mate in a big box store.

An international team of scientists, including biologists from the University of North Carolina (UNC) at Chapel Hill, may have pinpointed for the first time the mechanism responsible for cell polyploidy, a state in which cells contain more than two paired sets of chromosomes. When it comes to human chromosomes and the genes they carry, our tissue cells prefer matched pairs. Bundled within the nucleus of our cells are 46 chromosomes, one set of 23 inherited from each of our parents. Thus, we are known from a cellular standpoint as "diploid" creatures. But a cellular chromosome situation common in plants and in many insects is polyploidy, in which there are more – sometimes many more – than two sets of chromosomes. Here, growth occurs through an increase in cell size versus an increase in cell number via cell division (mitosis). This allows more DNA to be crammed into the cell nucleus. Polyploidy also appears in some tissues of otherwise diploid animals, including people – for example, in specialized organ tissue such as muscle, placenta, and liver. These biologically highly active tissues also produce large polyploid cells. An intriguing slice of discovery science led by geneticist Dr. Bruce Edgar, of the University of Heidelberg, Germany, was published online on Oct 30, 2011 in the journal Nature. The research team may have identified for the first time the regulatory mechanism responsible for cell polyploidy. Study co-author Dr. Robert J.

Researchers report they have figured out how the cancer-causing bacterium Helicobacter pylori attacks a cell's energy infrastructure, sparking a series of events in the cell that ultimately lead it to self-destruct. H. pylori are the only bacteria known to survive in the human stomach. Infection with H. pylori is associated with an increased risk of gastric cancer, the second-leading cause of cancer-related deaths worldwide. "More than half the world's population is currently infected with H. pylori," said University of Illinois microbiology professor Dr. Steven Blanke, who led the study. "And we've known for a long time that the host doesn't respond appropriately to clear the infection from the stomach, allowing the bacterium to persist as a risk factor for cancer." The new study, published in the September 20, 2011 issue of the Proceedings of the National Academy of Sciences, is the first to show how a bacterial toxin can disrupt a cell's mitochondria – its energy-generation and distribution system – to disable the cell and spur apoptosis (programmed cell death). "One of the hallmarks of long-term infection with H. pylori is an increase in apoptotic cells," Dr. Blanke said. "This may contribute to the development of cancer in several ways." Apoptosis can damage the epithelial cells that line the stomach, he said, "and chronic damage to any tissue is a risk factor for cancer." An increase in apoptotic cells may also spur the hyper-proliferation of stem cells in an attempt to repair the damaged tissue, increasing the chance of mutations that can lead to cancer. Previous studies had shown that VacA, a protein toxin produced by H. pylori, induces host cell death, Dr.